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Infants receiving long-term parenteral nutrition (PN) develop PN associated liver disease (PNALD). We previously showed that PN containing soy-based lipid supplemented with vitamin E (α-tocopherol) prevents the development of PNALD. We hypothesize that this occurs via vitamin E-activation of pregnane X receptor (PXR) mediated pathways involved in bile acid metabolism. Neonatal piglets received PN for 14 d containing Intralipid (IL, soy-based lipid emulsion), IL supplemented with 12.6 mg/kg*d vitamin E (VITE), or IL with 10 mg/kg*d Rifadin IV (RIF) a PXR agonist. Pigs treated with IL and VITE, but not RIF, developed cholestasis and hyperbilirubinemia, markers of liver disease. The hepatic PXR target genes CYP3A29 and UGT1A6 increased during RIF treatment. RIF also modestly increased metabolism of chenodeoxycholic acid to the more hydrophilic bile acid, hyocholic acid. Serum fibroblast growth factor (FGF)-19, a key regulator in suppressing hepatic bile acid synthesis significantly increased in the RIF group. We conclude rifampicin modified markers of PNALD development by increased metabolism of bile acids and potentially suppressed bile acid synthesis. Vitamin E was ineffective at high lipid doses in preventing PNALD.
This article was published in the following journal.
Name: American journal of physiology. Gastrointestinal and liver physiology
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Specialized solutions for PARENTERAL NUTRITION. They may contain a variety of MICRONUTRIENTS; VITAMINS; AMINO ACIDS; CARBOHYDRATES; LIPIDS; and SALTS.
A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
The administering of nutrients for assimilation and utilization by a patient who cannot maintain adequate nutrition by enteral feeding alone. Nutrients are administered by a route other than the alimentary canal (e.g., intravenously, subcutaneously).
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